Etomidate Pharmacology

Etomidate pharmacology is studied using following points. In etomidate pharmacology we find that Etomidate is a potent, direct cerebral vasoconstrictor. It decreases cerebral blood flow and CMRO2 in an independent manner.

The cerebral metabolic effects of etomidate are secondary to its effect on neuronal function. As a result, previously increase ICP is lowered by etomidate in etomidate pharmacology and in most regions CBF decreased significantly after etomidate.

Etomidate pharmacology also possesses anticonvulsant properties and therefore, may be useful in the treatment of status epilepticus. In hypoxic-ischaemic conditions etomidate has some protective effects, due to its anticonvulsant action, and lowering of the CMRO2, as well as reducing the rise of intracranial pressure.

In dogs, a bolus or infusion produces high amplitude theta activity on the electroencephalogram (EEG). During infusion, burst suppression is seen. After high doses, behaviour and LEG changes returned to normal within 3 hours.

Etomidate is epileptogenic and may activate seizure foci, therefore should be used with caution in patients with focal epilepsy. Bolus administration of etomidate (0.1 mg/kg) augments the somatosensory evoked potentials (SSEP) amplitude in incremental doses.

Thus, intermittent injection of etomidate in etomidate pharmacology can be used to augment small SSEP waves with reproducible increases in wave amplitude.

Cardiovascular System

Cardiovascular stability is characteristic of induction of anaesthesia with 0.3 mg/kg IV of etomidate under etomidate pharmacology After this dose ofetomidate, there are minimal changes in heart rate, stroke volume, or cardiac output, whereas mean arterial blood pressure may decrease up to 15—20% because of decreases in systemic vascular resistance.

The decrease in systemic blood pressure in parallel with change in systemic vascular resistance and is dose dependent. In etomidate pharmacology the etomidate does not cause any change in niyocardial blood flow distribution and myoqatdial metbolisrw of lactate, glucose and free fatty acids. Pascoe et al. ddcumented minimal changes in cardiopulmonary function with etomidate when administered to hypovolaemic dogs.

Etomidate does not affect pulmonary arterial pressure and vascular resistance, central venous pressure and pulmonary capillary wedge pressure. As per the etomidate pharmacology the etomidate possesses significant platelet inhibitqry properties which may be significant in patients with bleeding disorders.

Price et al. demonstrated a decrease of 16% in cardiac index after induction with etomidate. Etomidate maintains haemodynamic stability through preservation of both sympathetic outflow and autonomic reflexes (baroreflex). Effects of etomidate on myocardial contractility are important to consider, as this drug has been proposed for induction of anaesthesia in patients with little or no cardiac reserve.

In this regard, etomidate causes dose-dependent decreases in developed tension in isolated cardiac muscle obtained from patients undergoing coronary artery bypass graft operations or cardiac transplantation. Also in etomidate pharmacology this depression was reversible with beta-adrenergic stimulation.

Nevertheless, concentrations required to produce these negative inotropic effects are in excess of those achieved with clinical use. In contrast to other IV anaesthetics, as we know that in etomidate pharmacology the etomidate does not greatly decrease renal blood flow.

Etomidate pharmacology causes less respiratory depression than barbiturates. Like other intravenous agents transient apnoea may occur. It decreases tidal volume and minute volume; however, a compensatory increase in the frequency of breathing causes minimal effect on the blood-gas values.

Etomidate like methohexital similarly depresses the medullary respiratory centers; however, ventilation at any given CO2 tension is greater after etomidate than after methohexital, which indicates that etomidate may cause a C02-independent stimulation of ventilation, suggesting its use for induction of anaesthesia in cases where maintenance of spontaneous ventilation is desirable.

In etomidate pharmacology the depression ventilation may be exaggerated when etomidate is combined with inhaled anaesthetics or opioids during continuous infusion techniques.

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